Grants and Contracts Details
Over the years, the importation of carrier stallions and virus infective semen into the US unquestionably has been responsible for the introduction of new strains of equine arteritis virus (EA V) and the occurrence of new outbreaks of equine viral arteritis (EVA)'·I7·". Experience over the past 20 plus years would indicate that, EA V infection is of increasing economic significance to the $102 billion/annum horse industry in the US. Following EA V infection, a variable proportion up to 30-70% of stallions can become persistently infected and continuously shed the virus in their semen". In 2006, a multistate occurrence of EVA was confirmed in Quarter horses for the first time resulting primarily from the shipment of virus infective semen and the interstate movement of donor or embryo recipient mares". During this occurrence of EVA in the American Quarter horse population, EA V also spilled over into other breeds of horses (Thoroughbreds [TBl, Warrnbloods, Arabian, American Saddlebred [SBl, Paint, Andalusian) and led to establishment of the carrier state in a number of stallions". This recent outbreak in American Quarter horses has enhanced the existing EA V carrier reservoir and perpetuation of the virus in the Quarter horse breeding population. Recently, we also have demonstrated that virus can be transmitted during embryo transfer following insemination with EA V infective semen from carrier stallions'. Studies in our laboratory have shown that an in vitro assay based on dual flow cytometry analysis of CD3+ T cells (a white blood cells subset in the blood) could be used to predict horses that are highly susceptible to EAV infection'. Based on the phenotype of CD3+T cell sUbpopulation to in vitro infection with EAV, the horses could be divided into susceptible and resistant groups. Recently, we have extended these studies and established the possible correlation between susceptibility of CD3+ T lymphocytes to EA V infection and establishment of persistent infection in stallions (see preliminary data). Interestingly, the data suggested that carrier stallions that have phenotype of susceptible CD3+ T lymphocytes to EA V infection may represent those at higher risk of becoming persistently infected compared to stallions that they do not possess this phenotype. Therefore, now we would like to identify a genetic marker(s) that correlates with the establishment of EA V carrier state by analyzing genetic profiles of EA V carrier and non carrier stallions. By identifying the genetic determinants involved in establishment of carrier status of EAV. we may be able to develop a genetic test to identify stallions that are predisposed to persistent infection. Results of this study will enhance our understanding of the carrier state. as well as susceptibility to the disease.
|Effective start/end date||5/1/11 → 4/30/12|
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